Abstract
Background
MSA is clinically classified into two phenotypes: parkinsonism predominant (MSA‐P) and cerebellar ataxia predominant (MSA‐C). However, little is known about the differences in urinary dysfunctions between MSA‐C and MSA‐P. We investigated the differences in urinary and cardiovascular dysfunctions between MSA‐C and MSA‐P.
Methods
We retrospectively reviewed the medical records of patients with MSA diagnosed as having probable or possible MSA according to Gilman's second consensus criteria from January 2007 to September 2013 in our hospital. Data regarding the initial symptoms, onset of urinary symptoms, and results of urodynamic (including anal sphincter electromyography) and head‐up tilt tests were collected.
Results
A total of 100 patients with MSA, including 59 patients with MSA‐C and 41 with MSA‐P, were reviewed. Initial symptoms were autonomic (n = 12) and cerebellar (n = 47) in the MSA‐C phenotype and were autonomic (n = 14) and parkinsonian (n = 27) in the MSA‐P phenotypes. Urodynamic study indicated that bladder contraction was more severely impaired in patients with MSA‐P than in those with MSA‐C. In the head‐up tilt test, the decrease in diastolic blood pressure was significantly larger in the MSA‐P phenotype than that in the MSA‐C phenotype. Acontractile bladder during the pressure flow study increased likelihood that the phenotype is MSA‐P (odds ratio: 6.67; 95% confidence interval: 1.004–44.284; P = 0.050).
Conclusions
Urinary dysfunctions were more severe in MSA‐P compared with MSA‐C. Detailed urodynamic study was helpful for detecting subtle differences between MSA‐C and MSA‐P.
Keywords: multiple system atrophy, head‐up tilt test, urodynamic study
MSA is characterized clinically by any combination of autonomic symptoms, parkinsonism, and cerebellar ataxia.1, 2 Two clinical phenotypes of MSA have been established on the basis of the predominant motor symptoms: the parkinsonian variant (MSA‐P) and the cerebellar variant (MSA‐C). Although MSA‐P and MSA‐C may eventually show similar features in the advanced stage, the clinical symptoms are usually different, at least in the early stages. Recent increasing evidence has suggested that autonomic symptoms usually predate motor symptoms and that various autonomic symptoms could be detected in the early stages.3 We have previously reported that autonomic symptoms were prevalent in the early stage of MSA and urinary dysfunction was more common with earlier manifestation than orthostatic hypotension (OH).4 It is evident that urinary symptoms are prevalent and severe in patients with MSA according to previous studies on the natural history of MSA.5, 6, 7 However, most neurologists are unfamiliar with the clinical evaluation of urinary problems. It may not be rare that patients with MSA showing urinary symptoms without motor symptoms consult urological clinics and undergo urological surgery with poor outcomes.4 Difference in urinary dysfunction comprising the results of urodynamic study between MSA‐C and MSA‐P has never been examined in detail. A recent European cohort study revealed that the diagnosis of MSA‐P and incomplete bladder emptying predicted shorter survival,8 which suggests that it may be important to clarify urinary dysfunction in detail with respect to the clinical phenotype at an early stage for accurate prognosis.
Although OH is less prevalent compared with urinary dysfunction in patients with MSA,4 it is also a cardinal feature of MSA. In addition, we do not know the relationship between OH and urinary dysfunction with respect to clinical phenotype.
We aimed to clarify the differences in OH and urinary dysfunction between MSA‐C and MSA‐P by performing the head‐up tilt test and conducting the urodynamic study. We also evaluated the correlation between OH and urinary dysfunctions in both phenotypes that have never been studied using the results of the head‐up tilt test and urodynamic study.
Patients and Methods
We retrospectively reviewed the medical records of 100 patients with MSA who were diagnosed as having probable or possible MSA according to Gilman's second consensus criteria from January 2007 to September 2013 in Chiba University Hospital (Chiba, Japan).
Evaluation of Motor and Autonomic Dysfunction
All patients in this study were interviewed and examined carefully by neurologists who were experienced in the movement disorder field. Family members of the patients in this study were also interviewed to accurately evaluate the patients’ natural histories. Symptom onset was defined as the initial presentation of motor symptoms, including cerebellar and parkinsonian symptoms, or autonomic symptoms, including OH or pelvic organ symptoms. Locations of the initial motor symptoms (upper or lower limb) were also identified. For evaluation of the autonomic nervous system, cardiovascular autonomic symptoms were determined from interviews and OH was evaluated by performing the head‐up tilt test. Pelvic organ symptoms were basically evaluated using our original questionnaire.6, 9 Urinary dysfunctions were also evaluated by measuring postvoid residual urine volume (PVR) and conducting a urodynamic study. All patients in this study underwent brain MRI.
Head‐up Tilt Test and Heart Rate Variability
The head‐up tilt test was performed. Blood pressure and heart rate were measured using a sphygmomanometer at 1‐minute intervals. After 5 minutes of baseline measurement, each subject was passively tilted on an electrically driven tilt table at 70 degrees for 10 minutes. We diagnosed OH when patients showed a reduction in systolic blood pressure (SBP) of at least 20 mm Hg or that in diastolic blood pressure (DBP) of at least 10 mm Hg within 3 minutes of standing. For evaluating heart rate variability, electrocardiography was performed with the subjects in a supine position as 100 consecutive R‐R intervals with an accuracy of 1 ms during normal breathing in each subject. As an index of heart rate variability, the coefficient of variation of R‐R intervals (CVR‐R) was calculated as the standard deviatio divided by the mean R‐R interval. An abnormality in CVR‐R value was judged according to age (>1.18%; normal value as per the tests performed at our laboratory). CVR‐R was recorded during resting and deep breathing in each subject.
Urodynamic Study
A urodynamic study was conducted by neurologists and a urologist who were familiar with the free flowmetry and urodynamic study findings. The neurologists in this study carefully examined urinary dysfunction associated with neurological dysfunctions. The maximum and average flow rates were obtained by performing free flowmetry before conducting the pressure flow study. After the voided volume was measured, the PVR was measured using transurethral catheterization, and the normal volume was under 50 mL. Electromyography (EMG) cystometry was performed using a urodynamic computer (Janus; Life‐Tec Inc., Houston, TX) and an EMG computer (Neuropack Sigma; Nihon Kohden Inc., Tokyo, Japan). During the measurements, EMG of the anal sphincter was continuously recorded by inserting a coaxial needle electrode into the external anal sphincter (EAS) muscles. An 8F double‐lumen catheter was transurethrally inserted, and water (saline) cystometry was performed at an infusion rate of 50 mL/min while the patient was seated. Simultaneously, rectal pressure was measured using a balloon catheter and electronically subtracted from intravesical pressure. Water cystometry was followed by a pressure flow study. Both free flowmetry and a pressure flow study were performed in the sitting position in the same environment. Each flow study tracing was reviewed by the neurologists and urologist. Falsely high Qmax values observed in abdominal straining were excluded.
Abnormal urodynamic findings during the storage phase included detrusor overactivity defined as involuntary detrusor contractions during the filling phase. Quantitative parameters measured during the storage phase included the bladder volume at first desire to void (FDV) and strong desire to void (SDV): an FDV of <100 mL and an SDV of <300 mL were considered to be abnormal. Maximum cystometric capacity was the volume at which the patient could no longer delay micturition. Abnormal urodynamic findings during the voiding phase included impaired bladder contractility. Degree of detrusor contraction was evaluated using Schäfer's nomogram. Impaired detrusor contractility included “weak” and “very weak” contractility in Schäfer's nomogram. The methods, definitions, and units employed conformed to the standards recommended by the International Continence Society.10
EAS‐EMG
A disposable concentric needle electrode (needle diameter: 0.46 mm; Alpine Biomed, Skovlunde, Denmark) was inserted into the most superficial layer of the anal sphincter muscle under audio guidance. The needle was inserted into the right (5 o'clock position) and the left (7 o'clock position) sphincter muscles, and motor unit potential (MUP) analysis was separately performed. Five MUPs were recorded on each side. The position of the needle electrode was usually adjusted until continuous firing activities of three to five MUPs were visually observed. The rise time of the MUP was 300 to 500 μs. The range of sites from which MUP was recorded was approximately 1 cm from the anal orifice to a depth of 3 to 6 mm. A gain of 100 μV at 5 ms/div was used. The amplifier filter was set at 5 to 10 kHz.
MUPs were stored in the input buffer of the computer when the amplitude reached the threshold determined by the examiner. After visual confirmation that the three to five MUPs were continuously firing, the examiner manually set the threshold by moving the cursor to detect the visually confirmed three to five MUPs; subsequently, a total of 64 MUPs were stored in the input buffer of the computer. The stored 64 MUPs were classified into the four most similar MUPs using the auto MUP analysis software equipped with the EMG computer. The software identified the four most similar MUPs using the following procedures. The stored 64 MUPs were numbered as, for example, MUP1, MUP2, and MUP64. The auto MUP analysis software initially registered MUP1 as a template wave and calculated the correlational coefficient between MUP1 and MUP2. If the correlation coefficient exceeded 0.94, the software regarded MUP2 as identical to MUP1. Otherwise, MUP2 was regarded as a different wave from MUP1. The software repeated this procedure for the other MUPs and finally identified the four most similar MUPs. Our automated system could identify up to four MUPs, which were visually confirmed. The onset of the MUP was automatically determined when both the slope and the voltage exceeded predefined thresholds (onset slope: 5 μV/ms; onset level: 20 μV) above or below the baseline voltage in this study. Termination was also determined by the same procedure. Consequently, duration was automatically determined. Because this program could not identify late components (separate satellite potentials), the examiner checked the wave form and manually set the cursor to include late components. Late components were included in this “total MUP duration.” We repeated the above procedures to obtain 10 different MUPs by moving the position of the electrode. The EMG computer calculated mean duration, number of phases, and amplitude of the 10 different MUPs obtained.
Neurogenic change was diagnosed when mean duration of the MUPs was >10 ms, particularly including the late components. The method for performing EAS‐EMG and the diagnostic criteria of neurogenic change in EAS‐EMG were concurrent with those used in a previous study.9 All the EMG recordings were performed at Chiba University, and all the results in this study were examined using the same criteria. All our authors had an experience of working at Chiba University; therefore, they understood our duration criteria very well.
Statistical Analysis
The unpaired t test was used for comparison of PVR, mean duration of MUPs, and decrease in blood pressure in the head‐up tilt test between patients with MSA‐C and MSA‐P. Mann‐Whitney's U test was used to compare the degree of detrusor contraction (Schäfer's nomogram). Spearman's correlation coefficient was used for calculation of the relationship between disease duration and autonomic dysfunctions. Spearman's correlation coefficient was also used for calculation of the relationship between the decrease in blood pressure in the head‐up tilt test and urinary dysfunctions (PVR and mean duration of MUP). Multivariate step‐wise logistic regression analysis was performed to determine which parameters in the autonomic tests (decrease in blood pressure, PVR, mean duration of MUP, maximum systolic capacity, and bladder contractility evaluated by Schäfer's nomogram) were helpful for differentiation between MSA‐C and MSA‐P (a higher odds ratio [OR] suggested a diagnosis of MSA‐P in this analysis).
Standard Protocol Approvals, Registrations, and Patient Consents
This study was approved by the Chiba University Hospital Institutional Review Committee. Approval from an ethical standards committee to conduct this study was received.
Results
We reviewed a total of 100 patients with MSA, including 59 patients with MSA‐C (mean age: 65.5 ± 1.38; 39 males, 20 females; mean disease duration: 3.01 ± 0.3) and 41 with MSA‐P (mean age: 67.6 ± 0.95; 25 males, 16 females; mean disease duration: 3.01 ± 0.22). Figure 1 shows the frequencies of initial symptoms. In the MSA‐C group, the initial types of symptoms were autonomic in 12 (20%) patients (urinary, 14%; OH, 5%; erectile dysfunction [ED]: 2%) and cerebellar in 47 (80%) patients (dysarthria, 12%; upper limb: 3%; lower limb: 64%). In the MSA‐P group, the initial types of symptoms were autonomic in 14 (34%) patients (urinary, 24%; OH, 5%; ED, 5%) and parkinsonian in 27 (66%) patients (upper limb: 34%; lower limb: 32%).
Figure 1.
Initial symptoms of MSA‐C and MSA‐P. In patients whose initial symptom type was autonomic, urinary symptoms were most prevalent initially in MSA‐C (A) and MSA‐P (B).
Four patients with MSA‐C and 28 patients with MSA‐P were taking levodopa (mean l‐dopa equivalent dose was 332 ± 28 mg/day). Seven patients (MSA‐C, n = 6; MSA‐P, n = 1) were taking anticholinergic drug for urinary storage symptoms and 16 (MSA‐C, n = 9; MSA‐P, n = 7) were taking alpha‐blocker for urinary voiding symptoms. Two patients used clean intermittent self‐catheterization at the time of diagnosis.
Duration Between the Onset of Urinary Symptoms and Motor Symptoms, Urodynamic Findings, and EAS‐EMG
In the patients showing motor symptoms as initial symptoms, the onset of motor symptoms preceded that of urinary symptoms by 2.2 ± 0.25 years in patients with MSA‐C and by 2.1 ± 0.29 years in patients with MSA‐P, without significant difference (Table 1). Maximum intervals between onsets of urinary symptoms and initial motor symptoms were 6.0 years in MSA‐C and 4.7 years in MSA‐P, respectively. Mean PVR at time of examination was 148 ± 16 mL in MSA‐C and 152 ± 18 mL in MSA‐P, without significant difference (P = 0.37; Table 1).
Table 1.
Disease duration, urological findings and head‐up tilt test
| MSA‐C | MSA‐P | P Value (MSA‐C vs. MSA‐P) | MSA Total | |
|---|---|---|---|---|
| Disease duration | 3.01 ± 0.30 | 3.01 ± 0.23 | 0.98 | 3.01 ± 0.2 |
| Duration of urinary dysfunction (years) | 2.2 ± 0.25 | 2.1 ± 0.29 | 0.37 | 2.2 ± 0.18 |
| Postvoid residuals (mL) | 149.02 ± 16.2 | 152.93 ± 17.7 | 0.87 | 150.64 ± 11.9 |
| nEMG duration (ms) | 9.80 ± 0.31 | 9.72 ± 0.42 | 0.87 | 9.76 ± 0.24 |
| ⊿sBP (mm Hg) during HUT | 23.45 ± 2.88 | 26.76 ± 3.04 | 0.43 | 24.84 ± 2.09 |
| ⊿dBP (mm Hg) during HUT | 8.63 ± 1.98 | 15.63 ± 2.38 | 0.02a | 11.54 ± 1.55 |
| CVR‐R (%) | 1.76 ± 0.18 | 1.72 ± 0.15 | 0.66 | 1.75 ± 0.12 |
P < 0.02. nEMG: needle electromyography, HUT: Head‐up tilt test.
Of the 100 patients with MSA, a urodynamic study was conducted and an anal sphincter EMG was performed in 90 patients (52 patients with MSA‐C and 28 with MSA‐P). Detrusor overactivity was detected in 30 patients with MSA‐C (57%) and 15 with MSA‐P (51%), without statistical difference (P = 0.46; Fig. 2A). Bladder contraction evaluated by Schäfer's nomogram was significantly more severely impaired in patients with MSA‐P than in those with MSA‐C (P = 0.0069; Fig. 2B). In particular, prevalence of acontractile bladder was higher in patients with MSA‐P (n = 13; 35%) than in those with MSA‐C (n = 6; 12%; P < 0.05). In EAS‐EMG, mean duration of MUP was 9.79 ms in patients with MSA‐C and 9.71 ms in those with MSA‐P, without statistical significance (P = 0.87; Table 1).
Figure 2.
Urodynamic findings. Although the prevalence of detrusor overactivity was not significantly different (A), bladder contractility (evaluated by Schäfer's nomogram) was significantly impaired in MSA‐P compared with that in MSA‐C. Notably, MSA‐P had a higher prevalence of acontractile bladder than MSA‐C (B).
Head‐up Tilt Test and Heart Rate Variability
Mean decrease in SBP was 23.4 mm Hg in patients with MSA‐C and 26.7 mm Hg in those with MSA‐P, without statistical significance (P = 0.43; Table 1), whereas mean decrease in DBP was 8.6 mm Hg in patients with MSA‐C and 15.6 mm Hg in those with MSA‐P, with statistical significance (P = 0.02; Table 1). Mean value of CVR‐R (P = 0.60) was not significantly different between MSA‐C and MSA‐P (Table 1).
Correlation Between Disease Duration and Decrease in Blood Pressure in the Head‐up Tilt Test, PVR, and Duration of MUP in EAS‐EMG
We calculated the correlation coefficients between autonomic dysfunctions and disease duration. No significant correlation was observed between disease duration and PVR in the MSA‐C or MSA‐P group. The decrease in blood pressure in the head‐up tilt test and mean disease duration also did not show significant correlations in any group. In contrast, MUP duration in sphincter EMG showed significant positive correlation with disease duration in patients with MSA‐P (P = 0.04), but not in those with MSA‐C (Table 2).
Table 2.
Correlation between disease duration and autonomic dysfunction (decrease in blood pressure in the head‐up tilt test, PVR, and duration of MUP in EAS‐EMG)
| a) MSA‐C | Duration | b) MSA‐P | Duration | c) MSA Total | Duration | |||
|---|---|---|---|---|---|---|---|---|
| ⊿sBP | r | 0.03085 | ⊿sBP | r | −0.00126 | ⊿sBP | r | 0.0333 |
| P | 0.8214 | P | 0.9937 | P | 0.7461 | |||
| ⊿dBP | r | −0.07437 | ⊿dBP | r | 0.02981 | ⊿dBP | r | −0.01668 |
| P | 0.5859 | P | 0.8551 | P | 0.8718 | |||
| PVR | r | −0.12241 | PVR | r | −0.09544 | PVR | r | −0.10058 |
| P | 0.3688 | P | 0.558 | P | 0.3295 | |||
| nEMG duration | r | −0.08019 | nEMG duration | r | 0.35012 | nEMG duration | r | 0.0722 |
| P | 0.5759 | P | 0.0424a | P | 0.5114 | |||
P < 0.05. nEMG: needle electromyography.
The Head‐up Tilt Test and Its Correlation With PVR and Mean Duration of MUP in Anal Sphincter EMG
We calculated the correlation coefficients between PVR and the decreases in SBP or DBP during the head‐up tilt test in the MSA‐C and MSA‐P groups. In the MSA‐C group, PVR and blood pressure change did not show significant correlations, but there were significant positive correlations between PVR and the decrease in SBP (P = 0.01) or DBP (P = 0.02) during the head‐up tilt test in the MSA‐P group (Table 3). The decrease in DBP was significantly positively correlated with the mean duration of MUP only in patients with MSA‐C (P = 0.04).
Table 3.
Correlation between cardiovascular dysfunction and urinary dysfunction
| a) MSA‐C | b) MSA‐P | c) MSA Total | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| ⊿sBP | ⊿dBP | ⊿sBP | ⊿dBP | ⊿sBP | ⊿dBP | ||||||
| PVR | r | 0.11311 | 0.08509 | PVR | r | 0.3877 | 0.37014 | PVR | r | 0.2398 | 0.23225 |
| P | 0.42 | 0.5447 | P | 0.0134a | 0.0204a | P | 0.0206a | 0.0259a | |||
| nEMG duration | r | 0.10837 | 0.28205 | nEMG duration | r | 0.03211 | −0.01154 | nEMG duration | r | 0.10073 | 0.17337 |
| P | 0.4586 | 0.0496a | P | 0.857 | 0.9492 | P | 0.3649 | 0.1193 | |||
P < 0.05. nEMG: needle electromyography.
Multivariate Logistic Regression Analysis
To determine the usefulness of parameters in the autonomic tests (decrease in blood pressure, PVR, mean duration of MUP, bladder volume, and bladder contractility evaluated by Schäfer's nomogram) for differentiation between MSA‐C and MSA‐P, we performed multivariate logistic regression analysis. Acontractile bladder during the pressure flow study (Schäfer's nomogram) indicated that there is an increased likelihood that the phenotype is MSA‐P (OR, 10.00; 95% confidence interval [CI]: 1.280–78.117; P = 0.028). Other parameters were not significant as independent predictors of the diagnosis between patients with MSA‐C and MSA‐P (Table 4).
Table 4.
ORs for diagnosis of MSA‐P and of MSA‐C
| Bladder Contraction (Schäfer's Nomogram) | OR (95% CI) | P Value |
|---|---|---|
| Normal | Reference | |
| Weak | 1.556 (0.33–7.343) | 0.577 |
| Very weak | 0.333 (0.053–2.115) | 0.244 |
| Acontractile | 10.000 (1.28–78.117) | 0.028 |
Sex Differences
No sex differences were observed in any parameter (decrease in blood pressure, PVR, mean duration of MUP, and bladder contractility evaluated by Schäfer's nomogram).
Discussion
The present study revealed that 14% of patients with MSA‐C and 24% of patients with MSA‐P initially manifested urinary symptoms. Other patients initially developed motor symptoms, which preceded autonomic symptoms by 2.1 to 2.2 years. Prevalence of MSA in the patients who presented urinary symptoms as an initial symptom appeared to be slightly larger than that in a previous study; 8.8% to 19.1% of patients with MSA initially developed urinary symptoms.5, 11 Although all medical interviews were conducted by neurologists in our university hospital, our staff were trained to ask about urinary symptoms if the patients showed parkinsonism or cerebellar ataxia, a procedure that may have contributed to the high prevalence of urinary dysfunction as an initial symptom.
The time of onset of urinary dysfunction from initial motor symptoms, means of PVR, and MUP durations in EAS‐EMG were not significantly different between the MSA‐C and MSA‐P groups. Bladder contractility, as evaluated by Schäfer's nomogram, was significantly impaired in the patients with MSA‐P relative to that in those with MSA‐C. Multivariate logistic regression analysis revealed that an acontractile bladder during the pressure flow study indicates that there is an increased likelihood that the phenotype is MSA‐P. In the head‐up tilt test, the decrease in diastolic pressure was significantly larger in patients with MSA‐P than in patients with MSA‐C, whereas the mean decreases in SBP were not significantly different between the groups.
PVR did not show significant correlations with disease duration in either group, whereas MUP duration showed a significant positive correlation with disease duration only in the MSA‐P group. Disease duration did not show significant correlations with the decreases in SBP or DBP in the two groups.
Concerning the relationship between urological (PVR and MUP duration) dysfunctions and OH, the decrease in DBP had significantly positive correlations with MUP duration in patients with MSA‐C, whereas the decrease in SBP and DBP had positive correlations with PVR in patients with MSA‐P.
Unexpectedly, disease duration and PVR did not show significant correlation in either the MSA‐C or MSA‐P group, which suggests that the severity and progression of urinary dysfunction were heterogeneous in patients with MSA. These results may be attributable to the cross‐sectional analysis in this study. Our previous longitudinal study revealed that both urinary symptoms and PVR worsened with disease progression.9
The present results suggested that urinary dysfunctions and OH were slightly more severe in patients with MSA‐P than in those with MSA‐C because of the larger decrease in DBP in the head‐up tilt test and impaired bladder contractility, as evaluated by Schäfer's nomogram, in the urodynamic study. A recent European cohort study also showed that diagnosis of MSA‐P and incomplete bladder emptying predicted shorter survival.8 However, the difference in incomplete bladder emptying between MSA‐C and MSA‐P was evident only by the urodynamic study findings (Schäfer's nomogram) in this study. These results suggested that the subtle difference in incomplete bladder emptying could not be elucidated only by measuring PVR.
The decreases in the SBP and DBP in the head‐up tilt test were correlated with the PVR in MSA‐P, which suggested that the progression of OH and urological dysfunctions was parallel in patients with MSA‐P. However, we do not know exactly why the OH and PVR did not show significant correlation in the MSA‐C group. It is possible that OH and urologic dysfunctions are dissociated in MSA‐C. However, because we did not perform detailed cardiovascular autonomic function, such as 123I‐metaiodobenzylguanidine scintigraphy, Valsalva maneuver, norepinephrine supine, and standing, we could not refer to the relationship between the cardiovascular and urinary dysfunctions.
Several previous studies that have examined the differences in autonomic dysfunctions between MSA‐C and MSA‐P concluded that autonomic symptoms may not be different between MSA‐C and MSA‐P.11, 12 However, Wenning et al. concluded that OH appeared to be tightly linked with MSA‐C, which probably reflected differences in brainstem pathology,13 but the present study results did not support that conclusion.
Differences in PVR and detailed urodynamic findings between MSA‐C and MSA‐P have not been previously reported. The present study indicated that slight differences in urinary dysfunctions between MSA‐C and MSA‐P may be elucidated by performing urodynamic study.
The previous study has found that up to 50% patients with MSA report that the presentation of the disease was autonomic only.11 Because some reports have concluded that severe autonomic dysfunctions were negative prognostic factors,8, 14 detailed autonomic examinations should be helpful for accurately predicting prognosis in MSA.
Conclusions
Urinary dysfunctions were slightly more severe in MSA‐P compared with MSA‐C. Detailed urodynamic study was helpful for detecting subtle differences between MSA‐C and MSA‐P.
Author Roles
(1) Research Project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript Preparation: A. Writing of the First Draft, B. Review and Critique.
T.Y.: 1A, 1B, 1C, 2A, 1B, 2C, 3A
M.A.: 1A, 1B, 3A
Y.Y.: 1A, 1B
T.U.: 1A, 1B
S.H.: 1A, 1B
A.S.: 1A, 1B
R.S.: 1A, 1B
S.K.: 2C, 3B
Disclosures
Funding Sources and Conflicts of Interest: The authors report no sources of funding and no conflicts of interest.
Financial Disclosures for previous 12 months: The authors declare that there are no disclosures to report.
Relevant disclosures and conflicts of interest are listed at the end of this article.
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